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首页> 外文期刊>The European Journal of Neuroscience >Gene expression changes in thalamus and inferior colliculus associated with inflammation, cellular stress, metabolism and structural damage in thiamine deficiency.
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Gene expression changes in thalamus and inferior colliculus associated with inflammation, cellular stress, metabolism and structural damage in thiamine deficiency.

机译：硫胺素缺乏症的炎症，细胞应激，代谢和结构损伤相关的丘脑和下丘脑基因表达变化。

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Abstract Identification of gene expression changes that promote focal neuronal death and neurological dysfunction can further our understanding of the pathophysiology of these disease states and could lead to new pharmacological and molecular therapies. Impairment of oxidative metabolism is a pathogenetic mechanism underlying neuronal death in many chronic neurodegenerative diseases as well as in Wernicke's encephalopathy (WE), a disorder induced by thiamine deficiency (TD). To identify functional pathways that lead to neuronal damage in this disorder, we have examined gene expression changes in the vulnerable thalamus and inferior colliculus of TD rats using Affymetrix Rat Genome GeneChip analysis in combination with gene ontology and functional categorization assessment utilizing the NetAffx GO Mining Tool. Of the 15 927 transcripts analysed, 125 in thalamus and 141 in inferior colliculus were more abundantly expressed in TD rats compared with control animals. In both regions, the major functional categories of transcripts that were increased in abundance after TD were those associated with inflammation ( approximately 33%), stress ( approximately 20%), cell death and repair ( approximately 26%), and metabolic perturbation ( approximately 19%), together constituting approximately 98% of all transcripts up-regulated. These changes occurred against a background of neuronal cell loss and reactive astro- and microgliosis in both structures. Our results indicate that (i) TD produces changes in gene expression that are consistent with the observed dysfunction and pathology, and (ii) similar alterations in expression occur in thalamus and inferior colliculus, brain regions previously considered to differ in pathology. These findings provide important new insight into processes responsible for lesion development in TD, and possibly WE.
机译：摘要鉴定促进局灶性神经元死亡和神经功能障碍的基因表达变化，可以进一步加深我们对这些疾病状态的病理生理学的了解，并可能导致新的药理和分子疗法。氧化代谢障碍是许多慢性神经退行性疾病以及维尼克脑病（WE）（由硫胺素缺乏症（TD）引起的疾病）中神经元死亡的潜在发病机制。为了确定导致这种疾病的神经元损伤的功能途径，我们使用Affymetrix大鼠基因组GeneChip分析结合基因本体论和功能分类评估（使用NetAffx GO挖掘工具），检查了TD大鼠脆弱丘脑和下丘的基因表达变化。在分析的15927个转录本中，与对照组相比，TD大鼠中丘脑中的125个和下丘中的141个表达更为丰富。在这两个地区，TD后大量增加的转录本的主要功能类别是与炎症相关的那些（约33％），压力（约20％），细胞死亡和修复（约26％）以及代谢紊乱（约19％），约占所有上调转录本的98％。这些变化发生在两个结构中神经元细胞丢失以及反应性星形胶质和小胶质细胞减少的背景下。我们的结果表明（i）TD产生的基因表达变化与观察到的功能障碍和病理学一致，并且（ii）丘脑和下丘脑（以前被认为在病理学上不同）的大脑区域发生了类似的表达变化。这些发现提供了重要的新见解，可了解导致TD甚至WE病变发展的过程。

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